Feline Leukaemia Virus

Oswald Jarrett, University of Glasgow, Glasgow, UK
James C Neil, University of Glasgow, Glasgow, UK

Published online: April 2012

DOI: 10.1002/9780470015902.a0001021.pub2

Feline leukaemia virus (FeLV) is a gammaretrovirus that causes a variety of fatal diseases including leukaemia and lymphoma in its host, the domestic cat, and occasionally in large cat species. Many cats become persistently infected and develop disease after an incubation period of several years, during which virus can be transmitted to other cats. Disease is often associated with the generation of FeLV variants with increased pathogenic potential that can arise by mutation of envelope sequences, duplication of transcriptional enhancer elements or recombination with host proto‐oncogene sequences. FeLV can also produce variants by recombination with endogenous proviruses related to FeLV that are found in the domestic cat and its close relatives. The prevalence of FeLV infection has been reduced in many cat populations by isolation of infected carriers and more recently by vaccines that augment the natural ability of most cats to control infection.

Key Concepts:

  • The outcome of infection by FeLV depends on the infectious dose, age and immunocompetence of the host. Many cats achieve lifelong control, if not elimination of infection.
  • Cats that become persistently viraemic are at risk of a variety of FeLV‐related diseases after a latent period of up to several years.
  • The common infectious form, FeLV‐A can acquire altered entry receptor specificity by envelope gene mutation (to FeLV‐C) or recombination with endogenous FeLV‐related proviruses (to FeLV‐B).
  • FeLV envelope variants may induce fatal diseases of rapid onset including nonregenerative anaemia (FeLV‐C) or wasting and immunodeficiency (FeLV‐T).
  • The oncogenic potential of FeLV can evolve by duplication of transcriptional enhancer control elements in the long‐terminal repeat or by transduction of host proto‐oncogene sequences.
  • Although the immune parameters of vaccine protection remain unclear, FeLV demonstrates the feasibility of effective immunisation against the gamma retroviruses.
  • Commercial FeLV vaccines in recent or current use include inactivated FeLV, infected cell extracts, recombinant envelope protein and live recombinant poxvirus vaccines.

Keywords: retrovirus; FeLV; oncogene; transduction; endogenous retrovirus; receptor; transporter; leukaemia; lymphoma; immunodeficiency

Figure 1. The natural history and epidemiology of infection with FeLV and its variants. The common infectious form of FeLV (FeLV‐A) is conserved in antigenic structure and of low pathogenicity. Most exposed cats control initial infection, whereas those that become persistently viraemic are at risk of developing fatal disease that may be associated with the evolution of a variant FeLV as shown (see Figure 2). Contact transmission studies have shown that variants are not efficiently transmitted by natural spread.
Figure 2. Origin and molecular structure of FeLV variants. FeLV‐B, C and T are envelope variants generated by mutations (C, T) or recombination with endogenous FeLV (B). FeLV‐onc are generated by recombination with cellular proto‐oncogene sequences (e.g. Myc, Abl, Fes, Fms and Kit), whereas FeLV‐LTRen+ are generated by duplication of enhancer sequences in the long‐terminal repeats.
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 Further Reading
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    Rohn JL, Gwynn SR, Lauring AS, Linenberger ML and Overbaugh J (1996) Viral genetic variation, AIDS, and the multistep nature of carcinogenesis: the feline leukemia virus model. Leukemia 10: 1867–1869.

Related Sub-Topics:

Virus Diseases | RNA Viruses | Viruses Infecting Animals
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Article Title: Feline Leukaemia Virus
 
How to Cite close
Jarrett, Oswald, and Neil, James C(Apr 2012) Feline Leukaemia Virus. In: eLS. John Wiley & Sons Ltd, Chichester. http://www.els.net [doi: 10.1002/9780470015902.a0001021.pub2]